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94 Cards in this Set
- Front
- Back
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Psychopharmacology
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study of drugs and behavior
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Why do people take psychoactive drugs?
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1. to feel good (pos. reinforcement causes DA release)
-psychological dependence -greatest amount occurs 2. to avoid feeling bad (reduce withdrawal) -neg. reinforcement; increases behavior -chemical dependence |
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absorption
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how we take drugs into the body
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distribution
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how the drug reaches its primary state of action
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taking drugs orally
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easiest, but problem with stomach acid
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injection
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subcutaneous: under skin
intramuscular intravenous: reaches brain in 10 sec (IV) quick response but most dangerous inhalation: reaches brain in 8 sec dermal: absorbed through skin buccal/nasal: under tongue |
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absorption
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all drugs that change how we feel must be able to cross the bbb (means can also cross the placental barrier)
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cocaine
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blocks reuptake of (increases activity at level of synapse in CNS)
monamine NT (most important DA...slows it down in other places) |
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nicotine
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acts as an agonist at nicotine cholinergic (ACh) receptors
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alcohol
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works on virtually every NT
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metabolism (detox/breakdown)
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how broken down and made into inactive forms that don't respond to nerons
--mostly done by liver (via enzymes) |
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Metabolic tolerance
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-enzyme induction (make more to break drug down more quickly)
-enzymes speed up chemical reaction -w/ repeated exposure enzymes get better so same amount of drug doesn't produce same effect (need more) |
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Cross tolerance
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tolerance to 1 drug results in tolerance to other drugs (usually that need similar enzymes for breakdown)
--ex: alcoholic shows up unconscious to ER and given barbiturate for surgery (same enzymes as alcohol) --liver disease would mean too much reaction |
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What if amount of drug is unchanged?
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-tolerance can still occur
-pharmacodynamic or physiological tolerance |
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acute alocohol
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-decreases glutamate and increases GABA
-body decreases GABA sensitivity (inhibition) to compensate |
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chronic alcohol
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-try to increase glutamate and decrease GABA
-upregulation of glutamate receptors -increase # or sensibility of glutamate receptors to compensate for decrease in activity and to get back to normal levels |
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alcohol withdrawal
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now have too many/sensitive glutamate receptors which means overexcitations, seizures, etc.
--only potentially lethal withdrawal |
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Environmental tolerance
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drugs taken in he same environment can also display tolerance associated with conditioned cues
---produces effects in anticipation of the drug ex:heroin-->constipation heroin WD-->diarrhea |
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Excretion (elimination)
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-how drug, once broken down (or not), is eliminated from the body
-most psychoactive drugs metabolites excreted in urine |
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Psychostimulants
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increase arousal; sympathetic nervous system
-cocaine -amphetamines --methamphetamine --drugs used to treat ADD ----Ritalin/Adderall |
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Behavioral effects of cocaine and/or amphetamine
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-stereotypic/repetitive behaviors
-appetite suppression/weight loss -possible aggression |
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Psychological dependence
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very strong for drugs that are smoked or injected
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Physical dependence
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-withdrawal, but could be other factors involved
-causes uncertain |
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formication
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think bugs are under skin
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Sedative hypnotics & anxiolytics (anxiety reducers)
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-produce relaxation, sleep, and ultimately unconsciousness and death from respiratory depression if dose is too high
-all work on GABA receptors to make GABA bind better and produce more inhibition |
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Effects of alcohol on the CNS
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-affects many NT systems
-inhibits glutamate activity -enhances GABA activity |
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Treatment for alcoholism
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-treat acute withdrawal (give drug)
-then, long term strategies: pharmacotherapies, AA |
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Alcohol withdrawal
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-down regulation of GABA
-up regulation of glutamate -treat with benzodiazepenes to reduce the risk of seizures |
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Behavioral effects of nicotine
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-rewarding, pleasurable because of DA
-paradoxical effects on arousal --increased attention at lower doses --decreased anxiety/arousal at higher doses -decreased hunger and weight reduction (NT release and increased metabolism b/c of sympathetic NS activation) |
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How does nicotine exert behavioral effects?
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-nACh receptors: nicotine subtype of ACh
-found in PNS -autonomic (so affects HR, BP, etc.) -muscles (all postsynaptic receptors are on muscles are nicotinic) -also CNS (hippocampus) |
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Biphasic effect
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low dose=stimulation
high dose=brief stimulation followed by blockade of transmission (why it's so addictive) |
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Treatment for nicotine dependence
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Pharmacotherapy:
-substitution therapy-provide nicotine via safer and less rewarding route (patch; gum) ---reduces the pos. reinforcing effects and provides neg. reinforcements (reducing withdrawal symptoms) Behavioral modification: -difficult; support groups |
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Benefits of nicotine
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-reduces risk of Parkinson's and Alzheimer's
-neuroprotective -reduces side effects of Schizophrenic meds (increases activity in cholinergic neurons) -can suppress autoimmune diseases |
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Pharmacodynamics of opiods
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-heroine, morphine, oxycodone, methadone
-activates endogenous opiate receptors -treatment uses substitution therapy |
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Methadone therapy (substitution)
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every day: replaces heroin, blocks withdrawal
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Buprenorphine therapy (substitution)
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every couple of days: blocks withdrawal, never abused b/c not as rewarding
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Hallucinogens
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-LSD (works on 5HT neurons)
-Amphetamine: ecstasy, has effect of 5HT, sometimes neurotoxic -Psychedelic anesthetics: PCP, ketamine (work on glutamate receptor) |
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How are drugs rewarding?
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may work like other reinforcers by releasing DA in reward circuits of the brain
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How can we tell if a drug has rewarding effects?
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self administration (in rats): press lever
fixed ratio, variable ratio (break point) conditioned place preference (one box had drugs, other didn't): allows us to learn about whether a drug has rewarding or aversive effects |
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Dopamine and reward
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-role suggested by self-stimulation studies (ESB)
-nucleas accumbens plays a primary role |
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DA antagonists
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-interfere with self-stimulation (ESB)
-reduce the reinforcing effects of food -reduce rewarding effects of cocaine and amphetamine |
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Stress
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nonspecific response of the body to any demand placed on it
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2 systems activated during stress/emotion
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1. sympathetic nervous system
2. HPA Axis - (hypothalamic-pituitary-adrenal) axis |
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Sympathetic nervous system during stress
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-activates adrenal glands to release E, NE, and other catecholamines into blood
-repeated activation may cause hypertension -lie detector tests; problems |
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HPA Axis - (hypothalamic-pituitary-adrenal) axis during stress
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-causes the release of "stress" hormones (corticisteroids)
-negative feedback loop |
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psychosomatic illnesses
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real illnesses that exacerbated by stress: can be potentially life threatening
-ulcers, heart disease, asthma, skin disease |
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Stress in the CNS: vervet monkeys
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gastric ulcers, overactive adrenal gland, degeneration and depletion of hippocampal neurons
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Chronic stress in humans and CNS
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Cushings Syndrome: increased glucocorticoid release (can be reversed with treatment)
PTSD Depressed patients |
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How might stress happen?
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increased cortisol-->increase of Ca+2 influx-->increased risk of overexcitation
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Immune system
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identifies and eliminates foreign materials that contact or enter body
--bacteria, viruses, parasites, donated organs also identifies and destroys cells that have undergone alterations (like unusual rates of cell division) -stress can disrupt immune function |
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Role of optimism
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associated with:
increased n of helper T cells increased natural killer cell activity |
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Lateralization of function
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function/behavior found in only one cerebral hemisphere
emotion, language, speech: -leaves space on other side -more efficient system to convey info b/c doesn't have to travel as far -but if there is injury in that region, no back up system for that behavior |
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Left hemisphere
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-analytical
-quantitative -language |
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Right hemisphere
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-music
-spatial abilities -artistic -emotions -facial recognition |
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Aphasia
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language deficit that can't be attributed to motor, motivational, sensory, or other explanations
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Broca's Aphasia
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-characterized by broken, halted speech (very slow), absence of prosody (motone, no flow/rhythm)
-comprehension and ability to read are fairly good -grammatical issues with connecting words |
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Broca's area
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-near primary motor cortex
-affects area that controls mouth -BUT, can't just be motor disorder |
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Wernicke's Aphasia
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-fluid aphasia, deficits appear to be in comprehension, words are nonsensical
-comprehension and reading ability are poor -prosody is there |
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Wernicke's area
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temporal lobe: close to primary auditory cortex
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Wada test
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-injection of sodium amytal or sodium amobarbital – anesthetic
-have patients count down to see if can still talk -used to determine which hemisphere is important for speech |
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split brain surgery
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-corpus callosum cut
--used to stop extreme seizure cases |
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consequences of split brain surgery
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-initially, odd behaviors (go away) b/c 2 sides of brain want different things
-subsequently, only can really tell by experimental manipulations in the lab |
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functional brain imaging
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fMRI or PET used to see which half is active when doing a language test
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Emotional facial expression
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-key for cues and survival
-right hemisphere: -recognition -display of emotion -brain damage (absence, but still feel things) -left side of face shows emotion sooner |
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chimera
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mirror image of half of face--left/left should show most emotion
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brain regions involved in emotion
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limbic system:
hypothalamus, hippocampus, amygdala, olfactory bulbs, septum sits within temporal lobe |
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Schizophrenia
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brain disease w/ genetic basis:
-enlarged ventricles (less brain mass) -prefrontal cortex (consequences, future planning) -hypofunctionality (reduced activity; concentration and attention) |
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Positive symptoms of Schizophrenia
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things you can see:
-hallucinations, delusions, etc. |
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Negative symptoms of Schizophrenia
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things that are absent:
-social withdrawal -cognitive symptoms--memory, attention, learning deficits |
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Twin studies for Schizophrenia
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monozygotic (one egg) twins--have 99% genes in common vs. dyzgotic twins--50% genes in common
--monozygotic twins have highest concordance rate |
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Family studies
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allows you to look at increased concordance rates (particularly in first-degree relatives)
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Adoption studies
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allows you to look at role of environment vs. genetics
(shows evidence that it's genetic) |
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Role of stress in Schizophrenia
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doesn't cause, but can make symptoms worse
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Role of viral exposure in Schizophrenia
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can activate immune & inflammatory cells that affect development of brain
i.e. flu |
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original pharmacological treatment for Schizophrenia
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-traditional neuroleptics, antipsychotics
relax, treats pos. symptoms (not neg) |
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Traditional Neuroleptics
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chlorpromazine (Thorazine) and haloperidol (Haldol):
-still most widely used and cheapest way to treat pos. symptoms -chlorpromazine has many other functions |
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main mechanism of action for schizophrenic meds
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-block DA receptors
-resulted in DA theory (too much) -D2 receptor subtype: --how well the drug binds to D2 receptor is linked to reduction in pos. symptoms |
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Evidence for the DA Theory for Schizophrenia
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-drugs that block DA decrease symptoms
-drugs that increase DA (coke, amphetamine) cause acute psychosis in regular people, worse for schizo -L-DOPA: Parkinson's treatment (helps with psychosis) -ephedrine (natural stimulant) |
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Major DA pathways in brain
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mesolimbic DA pathway – emotion
nigrostriatal DA pathway –movement mesocortical DA pathway – cognitive? |
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side effects with antipsychotic drugs
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-Parkinson like symptoms
-spastic muscle contractions in head and neck (dystonia) -restless, constant movement -tardive dyskinesia: permanent motor disorder, move mouth/tongue a lot |
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other NT affected by schizo drugs
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-block ACh: memory deficits, dry mouth, urinary retention
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atypical neuroleptics
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-first was clozapine: effective in proportion of patients that were unresponsive to previous meds
-reduced neg. symptoms -reduced tardive dyskinesias -side effect: agranulocytosis (potentially lethal drop in white blood cells) |
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What is different about atypicals?
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-some say the drugs bind to D2 receptors but also to a certain type of 5HT receptors
-some say these drugs do not bind quite as well to D2 receptors as the more traditional ones; but binds to other types of DA receptors -big step in treatment of Schizophrenia |
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Biological Factors Influencing likelihood of depression
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Genetics
concordance rates: fraternal twins - 20% concordance monozygotic or identical twins - 50% concordance |
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Tricyclic antidepressants
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Blocks reuptake of NE and 5HT
very widely used fairly significant side effects effects on other NT sedation, weight gain |
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MAO inhibitors
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-block enzyme that breaks down excess NE & 5HT
-proved as effective as traditional tricyclics or SSRIs -not used as first level txt due to risk of adverse side effects- related to diet |
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SSRIs
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Fluoxetine (Prozac) - first introduced in US in 1988
SSRIs have a more favorable side effect profile than earlier antidepressants relatively safe (esp in OD situations) some controversy…... – increased risk of suicide – especially in kids |
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dual action antidepressants
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SNRI – serotonin and norepinephrine reuptake inhibitors
may be more effective at treating somatic symptoms associated with depression ex. pain older tca with dual actions new antidepressants with dual actions |
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Current problems that still exist with pharmacotherapy of depression
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Some patients do not respond well to first treatment
most take 3 - 4 weeks to exert significant therapeutic effects |
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ECT - electroconvulsive therapy
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may cause the most rapid change in receptor density
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Sleep deprivation
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many sleep abnormalities associated with endogenous depression
reduced SWS, increased stage 1, increased REM |
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Phototherapy
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Seasonal Affective Disorder
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Bipolar
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shifts between manic and depressive states
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Bipolar treatment
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-lithium: extremely toxic
-anticonvulsants: increase GABA (inhibition) |
